ArticleThe oncologist2011
Choosing the best second-line tyrosine kinase inhibitor in imatinib-resistant chronic myeloid leukemia patients harboring Bcr-Abl kinase domain mutations: how reliable is the IC₅₀?
Article in The oncologist, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Under ONIOM Layers: Analysis of BCR-ABL Enzyme Inhibitors Through Bond-Critical Points and Natural Orbitals.Molecules (Basel, Switzerland) · 2025Article
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- Pyrimidine: A Privileged Scaffold for the Development of Anticancer Agents as Protein Kinase Inhibitors (Recent Update).Current pharmaceutical design · 2025Review
- Beyond IC50-A computational dynamic model of drug resistance in enzyme inhibition treatment.PLoS computational biology · 2024Article
- In Silico Molecular Modeling of Four New Afatinib Derived Molecules Targeting the Inhibition of the Mutated Form of BCR-ABL T315I.Molecules (Basel, Switzerland) · 2024Article
- Novel Phthalic-Based Anticancer Tyrosine Kinase Inhibitors: Design, Synthesis and Biological Activity.Current issues in molecular biology · 2023Article
- Solid Tumors and Kinase Inhibition: Management and Therapy Efficacy Evolution.International journal of molecular sciences · 2022Review
- Analysis of genetic variants in myeloproliferative neoplasms using a 22-gene next-generation sequencing panel.BMC medical genomics · 2022Article
- Overcoming Resistance to Kinase Inhibitors: The Paradigm of Chronic Myeloid Leukemia.OncoTargets and therapy · 2022Review
- Article
- A study of deregulated MMR pathways and anticancer potential of curcuma derivatives using computational approach.Scientific reports · 2021Article
- Inferring time-dependent population growth rates in cell cultures undergoing adaptation.BMC bioinformatics · 2020Article
- Article
- Stochastic modelling of tyrosine kinase inhibitor rotation therapy in chronic myeloid leukaemia.BMC cancer · 2019Article
- The molecular mechanisms underlying BCR/ABL degradation in chronic myeloid leukemia cells promoted by Beclin1-mediated autophagy.Cancer management and research · 2019Article
- Excellent outcomes of 2G-TKI therapy after imatinib failure in chronic phase CML patients.Oncotarget · 2018Article
- The Cure of Chronic Myeloid Leukemia: Are We There Yet?Current oncology reports · 2018Review
- Chronic myeloid leukemia: the paradigm of targeting oncogenic tyrosine kinase signaling and counteracting resistance for successful cancer therapy.Molecular cancer · 2018Review
- Article
- Best Practices in Chronic Myeloid Leukemia Monitoring and Management.The oncologist · 2016Review
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development of drug resistance to imatinib mesylate in chronic myeloid leukemia (CML) patients is often accompanied by selection of point mutations in the kinase domain (KD) of the Bcr-Abl oncoprotein, where imatinib binds. Several second-generation tyrosine kinase inhibitors (TKIs) have been designed rationally so as to enhance potency and retain the ability to bind mutated forms of Bcr-Abl. Since the preclinical phase of their development, most of these inhibitors have been tested in in vitro studies to assess their half maximal inhibitory concentration (IC₅₀) for unmutated and mutated Bcr-Abl-that is, the drug concentration required to inhibit the cell proliferation or the phosphorylation processes driven by either the unmutated or the mutated forms of the kinase. A number of such studies have been published, and now that two inhibitors-dasatinib and nilotinib-are available for the treatment of imatinib-resistant cases, it is tempting for clinicians to reason on the IC₅₀ values to guess, case by case, which one will work best in patients harboring specific Bcr-Abl KD mutations. Here, we discuss the pros and cons of using this approach in TKI selection.
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